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© 2006 American Society for Nutrition J. Nutr. 136:2201-2206, August 2006

Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

The Form of Dietary Conjugated Linoleic Acid Does Not Influence Plasma and Liver Triacylglycerol Concentrations in Syrian Golden Hamsters1,2

Trine Porsgaard3, Xuebing Xu4 and Huiling Mu3,*

3 Biochemistry and Nutrition Group and 4 Food Biotechnology and Engineering Group, BioCentrum-DTU, Technical University of Denmark, 2800 Lyngby, Denmark

* To whom correspondence should be addressed. E-mail: hm{at}biocentrum.dtu.dk.


   ABSTRACT
TOP
 ABSTRACT
Introduction
 Materials and Methods
 Results
 Discussion
 LITERATURE CITED
 
Several studies have shown that conjugated linoleic acid (CLA) supplementation can improve the plasma lipid profile and thereby probably decrease the risk for development of atherosclerosis. The aim of the present study was to compare the effects on plasma and organ lipids of different dietary forms of CLA: triacylglycerol (TAG), diacylglycerol (DAG), monoacylglycerol (MAG), and fatty acid ethyl esters (FAEEs). DAG-, MAG-, and FAEE-CLA were produced by enzymatic interesterifications and all supplements were composed of a 1:1 mixture of the 2 major CLA isomers: cis-9, trans-11 and trans-10, cis-12. Male Syrian Golden hamsters were fed mildly atherogenic diets (10 g butter/100 g, 0.1 g cholesterol/100 g) supplemented with 0.5 g CLA/100 g or without CLA (control) for 8 wk. Liver weights were greater in the TAG- and FAEE-CLA groups than in the control group. In general, the form of CLA did not differentially affect plasma or liver cholesterol or plasma lipoprotein cholesterol concentrations, but only the TAG-CLA group had a higher final plasma TAG concentration than the control group. Both CLA isomers were incorporated into plasma, livers, and spleens. The results of the present study suggest that the form in which CLA is supplemented in the diet does not affect hamster plasma and liver TAG concentrations. The TAG-CLA form, a frequently used form of supplemental CLA, increases plasma TAG concentrations. If similar effects occur in humans, supplemental TAG-CLA cannot be considered to be beneficial given the relation between plasma TAG and the development of atherosclerosis.


   Introduction
TOP
 ABSTRACT
 Introduction
Materials and Methods
 Results
 Discussion
 LITERATURE CITED
 
Conjugated linoleic acid (CLA)5 refers to a group of positional and geometric isomers of linoleic acid [18:2(n-6)]. CLA is produced naturally by bacterial hydrogenation and isomerization in the gut of ruminants (1), or they can be generated chemically by alkali isomerization of 18:2(n-6) (2). Many CLA isomers have been identified, but the 2 major isomers are the cis-9, trans-11 and trans-10, cis-12 isomers, where the former is the isomer occurring naturally in food. In most commercial CLA products, these 2 isomers are present in a 1:1 ratio. CLA has been reported to have various health-related benefits, including anticarcinogenic, antiatherosclerotic, lean body mass-enhancing, and immune function-enhancing effects (3).

One important but controversial observation is that CLA can decrease the extent of atherosclerosis in experimental animals (4–7), whereas similar effects were not that clear in human studies (8–11). A possible mechanism for the reduction in atherosclerosis is through the ability of CLA to alter hepatic lipid and lipoprotein metabolism (12–15). There are indications that the various CLA isomers may have different effects on the blood lipids and thereby affect the atherogenic potential differently (5,7,9,16). Although many positive effects have been found with CLA supplementation, some studies have shown concomitant enlargements of livers and spleens (17,18).

In most of the reported animal and clinical studies, the dietary CLA was supplemented either as triacylglycerols (TAGs) or free fatty acids in equimolar mixtures of the 2 major isomers, or as 1 of these isomers alone. The results from a small clinical study suggested that the form in which CLA was fed influenced the efficiency of CLA absorption because more CLA was absorbed into chylomicrons over 6 h when it was fed as TAGs and free fatty acids than as fatty acid ethyl esters (FAEEs) (19). In addition, in recent years, several experiments have shown that dietary diacylglycerols (DAGs) have metabolic characteristics distinct from those of TAGs that may contribute to the prevention of postprandial lipemia and obesity (20). One commercial product is on the market that combines the expected benefits of DAGs and CLA (CLA One DG; PharmaNutrients), although to our knowledge no documentation exists for the expected benefits.

Because of the reported health-related benefits of CLA, it is of major interest to maximize the effects of the ingested CLA. The aim of the present study was to investigate the effects on plasma, liver, and spleen lipids of different dietary CLA forms: TAGs, DAGs, monoacylglycerols (MAGs), or FAEEs with a 1:1 ratio between the isomers cis-9, trans-11 and trans-10, cis-12 CLA. These CLA forms were fed as part of mildly atherogenic diets to Syrian Golden hamsters.


   Materials and Methods
TOP
 ABSTRACT
 Introduction
 Materials and Methods
Results
 Discussion
 LITERATURE CITED
 
    Production and analysis of CLA forms. TAG-CLA was kindly donated by Cognis Deutschland. DAG-CLA was made through a glycerolysis reaction between TAG-CLA and glycerol with Novozym 435 in a solvent-free batch system (21). MAG-CLA was also made through a glycerolysis reaction between TAG-CLA and glycerol with Novozym 435 but in a continuous packed bed system with tert-butanol as medium (22). FAEE-CLA was made through an ethanolysis reaction in a batch system between TAG-CLA and ethanol as described previously (23). Short-path distillation was used for fractionation of the required products.

The concentration of TAG, DAG, and MAG in the TAG-, DAG-, and MAG-CLA forms was calculated by addition of known amounts of TAG 15:0, DAG 15:0, and MAG 13:0 to the CLA products, followed by lipid extraction with chloroform and methanol (24). The lipid extracts were separated into lipid classes on thin-layer chromatography (TLC) plates developed in heptane:isopropanol:acetic acid (95:5:1, by vol). The bands corresponding to TAG, DAG, and MAG were scraped off, methylated with BF3, and analyzed by GLC (25). The total fatty acid composition of each CLA product was determined by GLC after methylation with BF3 (25). CLA-FAEE was injected directly onto the GC.

    Animals, diets, and experimental design. The experiment was approved by the Danish National Committee for Animal Experiments and was conducted with 8- to 9-wk-old male Golden Syrian hamsters purchased from Harlan Scandinavia. The hamsters were housed individually in polyethylene cages in a temperature (21 ± 3°C)- and humidity (50 ± 15%)-controlled room with a 12-h day-night rhythm. The hamsters were fed a commercial pelleted hamster maintenance diet (Altromin 7020; proximate composition: protein, 19.0; fat, 4.2; fiber, 5.8; and carbohydrate, 50.3 g/100 g diet) during a 5- to 7-d acclimation period. The day before initiation of the experiment, they were deprived of food overnight. In the following morning, the hamsters were weighed as 91.8 ± 0.8 g and were anesthetized with 0.45 mL/100 g of a mixture composed of ketamin (50 g/L; Intervet International B.V.) and xylazin (20 g/L; Intervet International B.V.) in a 10:1.25 ratio (v:v). Blood was drawn from the retro-orbital venous plexus using EDTA-containing hematocrit tubes (Modulohm A/S) and plasma was isolated using a 1-15 Sigma hematocrit tube centrifuge. Following blood collection, the hamsters were given 0.02 mL/100 g of a 5 g/L atipamezol solution (Antisedan; Orion).

The hamsters were randomly divided into 5 groups of 9–10. For the following 8 wk, they were given free access to mildly atherogenic diets composed of powdered hamster maintenance diet (Altromin 7021; Brogaarden) with a similar composition as Altromin 7020, but supplemented with 10 g butter/100 g (purchased in a local supermarket), 0.1 g cholesterol/100 g (Sigma-Aldrich), and 0.5 g CLA/100 g either as TAG-, DAG-, MAG-, or FAEE-CLA. One group was not supplemented with CLA (control group). Diets were stored at –20°C and replaced every day. The hamsters were weighed weekly.

At the end of the experimental period, hamsters were fasted overnight, anesthetized with the ketamin-xylazin mixture, and blood was collected in EDTA-containing glasses by cardiac puncture. Livers, spleens, hearts, brains, and kidneys were dissected, weighed, and immediately frozen in liquid nitrogen. Plasma, except for 100 µL used immediately for lipoprotein cholesterol determinations, and organs were stored at –80°C until analysis.

    Plasma lipids. Cholesterol distribution among plasma lipoproteins was determined by online fast-phase liquid chromatography (FPLC) described by Kieft et al. (26) and Innis-Whitehouse et al. (27) with minor modifications. Briefly, the FPLC system consisted of a single Superose 6HR 10/30 column (Amersham Pharmacia Biotech), an online degasser (ERC), and the following equipment from Waters: a model 717 autosampler, 2 model 510 solvent pumps (pump A was used for the elution buffer with a flow rate at 0.35 mL/min, pump B for the enzymatic cholesterol reagent from Horiba ABX Diagnostics with a flow rate at 0.1 mL/min), and a model 490 detector operated at 500 nm. Elution was performed in a PBS solution, pH 7.4, containing 0.01% EDTA and 0.02% NaN3. The column effluent was combined with the enzymatic reagent through a zero dead-volume T-connector. The enzymatic reaction was carried out in a 6-m reaction coil in a thermostatted water bath at 37°C. An entire lipoprotein profile was completed within 65 min after injection of 20 µL of plasma. The cholesterol concentration in LDL and HDL was determined by external standards (LDL and HDL cal from Horiba ABX Diagnostics). The intra- and interassay CV were <3% using a reference human plasma sample. Because no standard was available for VLDL cholesterol, the areas obtained from the chromatograms were compared among the different groups.

The concentrations of total cholesterol and TAG in plasma were measured spectrophotometrically using enzymatic kits (ABX Pentra; Horiba ABX Diagnostics).

    Liver lipids. Liver TAG and cholesterol concentrations were measured by quantitative high-performance TLC using a slight modification of a method described by Müller et al. (28). Livers were added to linoleic acid methyl ester (Sigma) as an internal standard. Samples and a quantitative standard mixture composed of cholesterol, trilinolein, and linoleic acid methyl ester (a 6-point standard curve was applied on each plate) were applied on high-performance TLC plates and were developed in 2 runs in a solvent system consisting of hexane:diethyl ether:formic acid (80:20:1, by vol), increasing the length of the development by 2 cm in the second run in comparison with the first run.

    Fatty acid composition determinations. Fatty acid composition of TAGs and phospholipids (PLs) in plasma, liver, and spleen and in addition cholesterol esters (CEs) in liver was determined after extraction with chloroform and methanol (24), separation on TLC plates, methylation with BF3, and GLC analysis (25). Fatty acid composition of butter was determined after lipid extraction, methylation with KOH in methanol (29), and GLC analysis. Butter contained 0.5 g/100 g of cis-9, trans-11 CLA.

    Statistical analysis. Results are presented as means ± SEM, n = 9 or 10. Statistical analysis was performed using GraphPad PRISM version 3.02 (GraphPad software). Data were analyzed by one-way ANOVA followed by Tukey's multiple comparison post-test. Differences were considered significant at P < 0.05.


   Results
TOP
 ABSTRACT
 Introduction
 Materials and Methods
 Results
Discussion
 LITERATURE CITED
 
    Composition of dietary CLA products. The different dietary CLA products were enriched in TAG, DAG, MAG, or FAEE, respectively, as intended (Table 1). All 4 products contained the 2 main CLA isomers, cis-9, trans-11 and trans-10, cis-12, in a 1:1 ratio, and these 2 CLA fatty acids constituted just below 80 g/100 g of total fatty acids in the products.


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  		TABLE 1 Lipid class distribution and composition of major fatty acids in CLA products1

 
    Body and organ weights. Addition of CLA to the diet and the form in which CLA was added did not influence final body weights or weight gains (data not shown). Hamsters fed CLA in the form of TAG or FAEE had greater liver weights than the control group (P < 0.05). Spleen weight was greater in the DAG-CLA group compared with the control group (P < 0.05). Weights of other organs were not affected by dietary CLA (data not shown).

    Plasma lipids. Plasma total TAG and cholesterol concentrations before the feeding period were 1.03 ± 0.11 and 2.13 ± 0.04 mmol/L (n = 47), respectively. The plasma TAG concentration after 8-wk feeding tended to be higher in all CLA-supplemented groups compared with the control (P = {blacksquare}{blacksquare}{blacksquare}) and was higher in the CLA-TAG group (Fig. 1; P < 0.05). The plasma TAG concentrations in the other CLA-supplemented groups were intermediate and not different from the control or CLA-TAG groups. The final plasma total cholesterol concentration did not differ among any of the groups (data not shown).


Figure 1
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  		Figure 1  Total plasma TAG concentrations in Syrian Golden hamsters after 8 wk of consuming mildly atherogenic diets supplemented with 0.5 g/100 g CLA either as TAG, DAG, MAG, or FAEE, or with no CLA added (control). Values are means ± SEM, n = 9 or 10. Means without a common letter differ, P < 0.05.

 
The cholesterol concentration in plasma lipoproteins was easily determined by an online FPLC method that allowed fast determinations with only 20 µL of plasma. The effect of the mildly atherogenic diet was clearly visible in the chromatograms (Supplemental Fig. 1) with large increases in the VLDL and LDL cholesterol peaks, whereas the HDL cholesterol peak was less affected. Initial LDL and HDL cholesterol concentrations were 0.06 ± 0.01 and 2.27 ± 0.04 mmol/L (n = 47), respectively. The sum of the initial LDL and HDL cholesterol concentrations was 2.32 ± 0.4 mmol/L, a value higher than that measured using the enzymatic assay (2.13 ± 0.04 mmol/L). This indicated that the FPLC method slightly overestimated the cholesterol concentration because the VLDL cholesterol concentration also should be taken into consideration. This means that the absolute lipoprotein cholesterol concentrations may not be correct but the method we used allows comparisons among the groups.

VLDL cholesterol constituted 7.3 ± 0.8% of the total cholesterol area in the initial plasma samples, whereas the LDL cholesterol:HDL cholesterol ratio was 0.03 ± 0.00 (n = 47). After 8 wk, LDL cholesterol concentrations and VLDL cholesterol's contribution to the total cholesterol area were increased severalfold, whereas small increases in HDL cholesterol concentration occurred. Due to the large increases in LDL cholesterol, the LDL cholesterol:HDL cholesterol ratio increased severalfold as well. The dietary groups did not differ in final LDL and HDL cholesterol concentrations or in the LDL cholesterol:HDL cholesterol ratio, whereas the contribution of VLDL cholesterol to the total area (Fig. 2) was higher in the TAG- and DAG-CLA groups compared with the control group (P < 0.05).


Figure 2
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  		Figure 2  Contribution of VLDL cholesterol to total cholesterol in Syrian Golden hamsters after 8 wk of consuming mildly atherogenic diets supplemented with 0.5 g/100 g CLA either as TAG, DAG, MAG, or FAEE, or with no CLA added (control). Values are means ± SEM, n = 9 or 10. Means without a common letter differ, P < 0.05.

 
    Liver lipids. The concentration of TAG in liver after 8-wk supplementation with CLA in the form of TAG and DAG was higher than the concentration in livers of control hamsters but the 4 CLA-supplemented groups did not differ from one another (Fig. 3; P < 0.05). Hepatic cholesterol concentrations did not differ among the groups (data not shown).


Figure 3
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  		Figure 3  Total liver TAG concentrations in Syrian Golden hamsters after 8 wk of consuming mildly atherogenic diets supplemented with 0.5 g/100 g CLA either as TAG, DAG, MAG, or FAEE, or with no CLA added (control). Values are means ± SEM, n = 9 or 10. Means without a common letter differ, P < 0.05. The standard used in the assay was {blacksquare}{blacksquare}{blacksquare}, MW = {blacksquare}{blacksquare}{blacksquare}.

 
    Fatty acid compositions of plasma, liver, and spleen. The CLA isomers were incorporated to a higher degree into TAGs than into the PLs of plasma, liver, and spleen (Table 2). Furthermore, 2–4 times as much cis-9, trans-11 CLA compared with trans-10, cis-12 CLA was incorporated in both TAGs and PL of plasma and liver and in spleen TAGs, whereas the incorporation of both isomers in spleen PLs was generally very low and at a similar level. In plasma TAGs, the levels of both CLA isomers did not differ among the 4 dietary CLA groups but the CLA concentration was higher in all those groups than in the control group (P < 0.0001). In plasma PLs, the level of cis-9, trans-11 CLA was higher in the 4 CLA-supplemented groups compared with the control group (P < 0.0001), whereas, for the trans-10, cis-12 CLA isomer, the levels in DAG- and MAG-CLA groups were higher than in the control group (P < 0.05). Dietary CLA supplementation affected the levels of some of the (n-3) polyunsaturated fatty acids in plasma PLs. The 4 CLA-fed groups had lower levels of 20:5(n-3) (0.3–0.4 g/100 g fatty acid) than the control group (0.6 g/100 g, P < 0.001) and higher levels of 22:5(n-3) (1.3–1.4 g/100 g in the CLA groups versus 0.8 g/100 g in the control group) (P < 0.0001).


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  		TABLE 2 CLA concentrations in plasma, liver, and spleen of hamsters fed mildly atherogenic diets supplemented with 0.5 g/100 g CLA in the form of TAG, DAG, MAG, or FAEE, or without CLA addition (control) for 8 wk1

 
In liver, the highest CLA incorporation was in CEs, but only cis-9, trans-11 CLA was incorporated. The 4 CLA-fed groups had higher levels of the 2 CLA isomers in liver TAGs and PLs than the control group, except for trans-10, cis-12 CLA incorporation in TAGs, which was only higher in the DAG-CLA and MAG-CLA groups (P < 0.001). Like in plasma PLs, CLA supplementation changed the levels of some of the long-chain polyunsaturated fatty acids. The 4 CLA-fed groups had lower levels of 20:4(n-6) and 20:5(n-3) (8.9–9.4 and 0.3 g/100 g fatty acid, respectively) than the control group (11.0 and 0.6 g/100 g fatty acid, respectively; P < 0.0001), but higher levels of 22:5(n-6) and 22:6(n-3) (0.7 and 1.5–1.6 g/100 g fatty acids in the CLA-supplemented groups versus 0.4 and 0.9 g/100 g in the control group; P < 0.001).


   Discussion
TOP
 ABSTRACT
 Introduction
 Materials and Methods
 Results
 Discussion
LITERATURE CITED
 
A number of studies in hamsters have shown that CLA supplementation can improve the plasma lipid profile and thereby probably decrease the risk for development of atherosclerosis (5–7,30), although controversy exists as to which isomer is the active agent.

In contrast, in the present study, when a 1:1 mixture of cis-9, trans-11 CLA and trans-10, cis-12 CLA was added to a mildly atherogenic diet of Syrian Golden hamsters in the form of TAG-, DAG-, MAG-, or FAEE-CLA, it had no beneficial effects on either total or lipoprotein cholesterol levels in comparison with a group fed the same diet but without CLA supplementation. In addition, TAG-CLA increased total plasma TAG, and TAG- and DAG-CLA increased VLDL cholesterol and the liver TAG concentration in comparison with the control group; these effects cannot be considered beneficial with regard to the development of atherosclerosis. Similar to our experiment, hamsters fed atherosclerotic diets supplemented with the 2 CLA isomers separately did not result in any beneficial changes in the lipoprotein profile, but both isomers reduced atherosclerotic lesion development (6). Wilson et al. (4) observed not only an increase in plasma TAG concentrations in hamsters fed hypercholesterolemic diets supplemented with a CLA mixture, but also a reduced aortic fatty streak formation. Atherosclerotic lesion development was not measured in the present experiment, but the changes in plasma lipids observed in different studies are seemingly not consistent and do not appear to correlate with the presence of atherosclerosis. The discrepancies between the different experiments may be due to a number of factors, including strain, age of the hamsters, amount and type of CLA, the duration of supplementation, and the other dietary components. Furthermore, in agreement with our results, limited effects of CLA mixtures on blood lipids were reported in clinical studies as reviewed by Terpstra (8), although 1 of the recently published studies has indicated opposing effects of the individual isomers on human plasma lipids, with trans-10, cis-12 CLA exerting hyperlipidemic properties and cis-9, trans-11 CLA hypolipidemic properties (9).

Because liver TAGs, total plasma TAGs, and VLDL cholesterol were higher in the TAG-CLA group compared with the control, this supplemental form of CLA increased VLDL production in the liver and thereby the VLDL concentration in plasma. Supplemental CLA is most often sold as TAGs or free fatty acids but, from the results reported in the present experiment, other forms of CLA may be preferable, although none of the investigated forms produced beneficial effects on plasma and liver lipids with regard to the development of atherosclerosis. On the other hand, MAG-CLA produced no undesired nutritional effects compared with the unsupplemented control group, and FAEE-CLA influenced liver weight but did not affect plasma and liver lipids in comparison with the control group. To our knowledge, only 1 previous study examined the effects of the form in which CLA was fed (19). In this small clinical study, more CLA was absorbed into chylomicrons over 6 h when it was consumed as TAGs and free fatty acids rather than as FAEEs.

CLA supplementation and the form of the supplemented CLA did not influence body weight gain in the present hamster study. On the contrary, CLA supplementation in the form of TAGs or FAEEs led to higher liver weights compared with the control group. The higher liver weights in the TAG-CLA group could partly be the result of an increased TAG concentration, but this could not be the only reason because the liver TAG concentration in the FAEE-CLA group was similar to the control group. Similar to what we observed with TAG- and DAG-CLA in the present study, CLA was found to increase liver lipids in hamsters (5), mice (18,31,32), and chickens (33), whereas in other studies no increases were found in hamsters (16) and rats (34). From cell culture studies, there were indications that the trans-10, cis-12 CLA isomer could decrease hepatic TAG secretion (35,36), but if the isomer decreased the secretion without decreasing its synthesis, it would lead to hepatic TAG accumulation. In other studies, increased liver weights in hamsters following CLA feeding were suggested to be due to hypertrophy caused by the trans-10, cis-12 CLA isomer (16) and an increased liver cell number induced by the same isomer (14). Liver cell number was not calculated in the present experiment, but it could also be a factor contributing to the increased liver weights in the TAG- and FAEE-CLA groups, although the underlying mechanisms are not clear.

DAG-CLA supplementation led to higher spleen weights compared with no CLA supplementation and, in general, CLA supplementation led to low incorporation of the 2 isomers into spleen PLs, and in contrast to the other analyzed tissues, the isomers were incorporated at a similar level. CLA supplementation (the 2 isomers separately or as a mixture) in mice was previously shown to increase spleen weight and it also influenced immunoglobulin production (17), whereas in rats no effect on spleen weight was observed, despite changes in immunoglobulin production caused by supplementation of a CLA mixture (37). These studies suggested that supplemental CLA may influence the function of the immune system and, from our results, the supplemental CLA form could influence the function, but this needs further investigation.

It has been reported previously that the incorporation of cis-9, trans-11 CLA was higher than that of trans-10, cis-12 CLA, and the incorporation of CLA isomers in TAGs was higher than in PLs in plasma and liver (14,16,32,38). The control group had incorporated measurable levels of cis-9, trans-11 in plasma and liver TAGs due to the concentration of this isomer in the dietary butter. The dietary CLA form had very limited influence on the incorporation of the 2 isomers in the analyzed tissues. In general, the control group had significantly lower concentration of the isomers compared with the groups supplemented with CLA. CLA supplementation influenced the metabolism of some of the long-chain polyunsaturated fatty acids in plasma and liver, probably due to the inhibition of retroconversion enzymes than altered desaturase activity. CLA supplementation was previously shown to influence desaturase activity in humans (38).

In conclusion, our results indicate that the form in which CLA is supplemented to the diet did not influence plasma and liver TAG concentrations in hamsters.


   ACKNOWLEDGMENTS
 
Karen Jensen, Grete Peitersen, Bert Nielsen, and Malene Leidecker are thanked for their technical assistance, and Lillian Vile and Nina Kjeldsen are thanked for help with the hamsters.


   FOOTNOTES
 
1 Supported by the Danish Technological Research Council. Back

2 Supplemental Figure 1 is available with the online posting of this paper at jn.nutrition.org. Back

5 Abbreviations used: CE, cholesterol ester; CLA, conjugated linoleic acid; DAG, diacylglycerol; FAEE, fatty acid ethyl ester; FPLC, fast-phase liquid chromatography; MAG, monoacylglycerol; PL, phospholipid; TAG, triacylglycerol; TLC, thin-layer chromatography. Back

Manuscript received 28 March 2006. Initial review completed 17 April 2006. Revision accepted 26 May 2006.


   LITERATURE CITED
TOP
 ABSTRACT
 Introduction
 Materials and Methods
 Results
 Discussion
 LITERATURE CITED
 

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